[27] This study did not examine the production of chemokines associated with airway neutrophil recruitment, but adds strength to the rationale for studying this molecule in the context of lung disease by demonstrating that S1P itself can induce airway hyperesponsiveness. Inhibition of mouse lung S1PR2 with JTE-013 inhibited S1P induced pulmonary vasoconstriction, another S1PR2/Rho kinase dependent phenomenon [28]. Here, S1PR2 is linked to lung disorder.